白细胞介素1受体拮抗剂等位基因与紫癜性肾炎和IgA肾病的相关…

目的为了进一步阐明紫癜性肾炎（ＨＳＰＮ）及ＩｇＡ肾病（ＩｇＡＮ）二者在发病机理上可能存在的联系，方法用ＰＣＲ方法对４３例ＨＳＰＮ，９７例ＩｇＡＮ患乾和９８名正常人ＩＬ－１受体拮剂（ＩＬ＿１ｒａ）基因数目可变的串联重复（ＶＮＴＲ）多态性进行了分析。结果ＨＳＰＮ患者白细胞介素１受体拮抗剂等位基因（ＩＬＲＮ２）的携带率明显高于正常人（Ｐ〈０．０２）和ＩｇＡＮ患乾中表现为反复发作性肉眼血尿患者戎ＩＬＩＲＡ     

复方丹参注射液联合东莨菪碱治疗以血尿为主要表现IgA肾病的临床观察

IgA肾病(IgAN)是我国主要的肾小球疾病之一,也是导致终末期肾衰竭的一个重要原因.其临床特点为反复发作性肉眼血尿或镜下血尿,可伴有不同程度的蛋白尿.现代医学对本病尤其是以血尿为主者尚无特效的治疗方法.我们根据IgAN患者存在微循环障碍的情况,应用复方丹参注射液联合东莨菪碱静脉滴注治疗60例以血尿为主要表现的IgAN患者,并设20例西药治疗进行对比,现报告如下.     

环境抗原在IgA肾病中的作用

系膜IgA肾病(IgAN)是临床上最常见的原发性肾小球疾病之一,阐明其发病机理是近20年来重点研究的课题。现认为IgAN不但是最常见的肾小球疾病之一,而且也是多见的发展至晚期肾功能衰竭的原因之一。本病的病因学还不清楚。许多研究证实肉眼血尿常随呼吸道和胃肠道感染发生而发作,也与巩膜外层炎、扁桃体切除术及牙齿治疗有关,有报道认为IgAN的发生与某些次食抗原有关。推测IgAN的发病可能与环境抗原所致的粘膜免疫有关。 Coppo等认为IgAN患者对IgA的产生具有高反应性,免疫系统的高反应性包括自身抗体的产生(抗核抗体或类风湿因子)对病毒疫苗及各种常见呼吸道和胃肠道微生物产生的高滴度抗体。IgAN患者肉眼血尿发作常与呼吸道和胃肠道感染有关,在其血清中可发现对细菌抗原及饮食抗原产生的高滴度抗体,认为这与全身免疫的高反应性有关,而     

胰岛素抵抗在IgA肾病中作用的研究进展

IgA肾病（IgA nephropathy,IgAN）又称Berger病,是一种自身免疫性肾病,是我国肾小球源性血尿最常见的病因,临床上以反复发作肉眼血尿或镜下血尿为特征。现在普遍认为年龄、体重、高血压、蛋白尿、高尿酸血症、     

成人单纯性血尿IgA肾病临床病理及相关危险因素分析

<正>IgA肾病(IgA nephropathy,IgAN)是常见的原发性肾小球疾病,预后不容乐观[1],临床以反复发作的肉眼血尿或镜下血尿为主要表现,可伴有少量蛋白尿,也可出现肾病综合征。目前关于不伴蛋白尿的单纯性血尿成人IgAN患者临床病理特点及血压、尿酸、血脂等相关危险因素对其的影响报道较少。了解这部分患者的病例特点,有助于更好地指导临床治疗,改善预后。     

白细胞介素在紫癜性肾炎发病机制中的作用研究进展

紫癜性肾炎(HSPN)继发于侵犯毛细血管的变态反应性疾病——过敏性紫癜(HSP)，肾脏受累是HSP常见而多变的表现，其发病率随所研究人群而不同。HSPN是儿科最为常见的继发性肾小球疾病，有报道，HSP是新月体肾炎最常见的病因。HSPN的特征之一是血尿，最常见是肉眼血尿，也可以见镜下血尿，血尿可以是一过性的或持续的或反复发作的。血尿可伴随紫癜出现或在肾外表现长时间消失后出现，常常与上呼吸道感染有关。HSPN通常还有不同程度的蛋白尿，肾病综合征的表现差异很大。已经证明，     

伴毛细血管襻纤维素样坏死IgA肾病的临床病理特点及预后分析

目的:回顾性分析伴毛细血管襻纤维素样坏死局灶增生性IgA肾病(IgAN)的临床病理特点及预后,探讨纤维素样坏死在IgAN的意义。方法:对55例伴纤维素样坏死局灶增生性IgAN患者的临床、实验室、病理表现及预后进行回顾性分析;并与同期60例不伴有纤维素样坏死的局灶增生性IgAN进行比较。结果:两组患者临床均可表现为隐匿性肾小球肾炎,肾炎综合征及肾病综合征。坏死组近一半的患者有前驱感染史及血IgA升高,多数患者24 h尿蛋白定量大于1 g,常伴发作性肉眼血尿。病理方面,坏死组伴发局灶新月体形成更常见。随访结束时,两组患者的肾脏生存率在随访期内差异无统计学意义。结论:伴纤维素样坏死的局灶增生性IgAN与对照组比较,尿蛋白大于1 g,前驱感染,发作性肉眼血尿及血IgA升高更常见。可出现肾功能异常。经积极治疗预后与非坏死组比较差异无统计学意义。     

胰岛素抵抗在IgA肾病中作用的研究进展

IgA肾病（IgA nephropathy,IgAN）又称Berger病,是一种自身免疫性肾病,是我国肾小球源性血尿最常见的病因,临床上以反复发作肉眼血尿或镜下血尿为特征。现在普遍认为年龄、体重、高血压、蛋白尿、高尿酸血症、肾衰竭、高血糖等均与IgAN的发生、发展密切相关。胰岛素抵抗（insulin resistance,IR）是指胰岛素作用的靶器官对胰岛素作用的敏感性下降,即正常剂量的胰岛素产生低于正常生物学效应的一种状态。     

伴有肉眼血尿的IgA肾病患者临床特征分析

目的:探讨病程中伴有肉眼血尿的IgA肾病患者的临床特征及其与血尿的关系。方法:根据病程中是否伴有肉眼血尿将经肾活检确诊的136例IgA肾病患者分为肉眼血尿组和无肉眼血组。分析对比两组在血压、24 h尿蛋白定量、血肌酐、尿素氮、血尿酸、血清IgA、尿液中乙酰β-D氨基葡萄糖苷酶(NAG)、尿β2-微球蛋白(β2-M)水平上的差异,并估算肾小球滤过率(eGFR)的差别。研究IgA肾病与血尿的关系。结果:(1)两组在性别和年龄上差异无统计学意义(P0.05),在病程上肉眼血尿组平均病程较无肉眼血尿组短(P0.05)。(2)肉眼血尿组前驱感染发生率显著高于无肉眼血尿组(P0.05)。(3)肉眼血尿组中高血压的发生率低于无肉眼血尿组(P0.05)。(4)在24 h尿蛋白定量上,肉眼血尿组24 h尿蛋白水平低于无肉眼血尿组,两组间差异有统计学意义(P0.05)。(5)肉眼血尿组血肌酐、尿素氮平均水平均低于无肉眼血尿组(P0.05)。(6)根据eGFR水平评估患者肾功能,肉眼血尿组肾衰竭发生率低于无肉眼血尿组。(7)两组在平均血尿酸、血清IgA、尿NAG酶和尿β2-M水平间差异性均无统计学意义(P0.05)。结论:在高血压发生率、24 h尿蛋白定量、尿素氮、血清肌酐水平和肾衰竭发生率上,病程中伴有肉眼血尿的IgAN患者均低于无肉眼血尿的IgAN患者,且伴有肉眼血尿的IgAN患者病程更短,提示其预后较不伴肉眼血尿者好,由于IgA肾病好发于青壮年,且多为体检时因血尿和(或)蛋白尿而偶然发现,因此诊治IgA肾病最佳的办法就是定期体检、及早发现和及时治疗。     

原发性IgA肾病402例临床与病理分析

目的分析不同类型IgA肾病（IgAN）的临床与病理特点。方法回顾性分析我院收治的402例IgAN患者。根据其临床表现将其分型,并对各类型的临床表现、组织病理、免疫病理进行回顾性分析。结果临床表现为反复发作性肉眼血尿型（R-GH）85例（21．1％）;单纯性肉眼血尿型（I-GH）19例（4．7％）;无症状性尿检异常（Uab）135例（33．6％）;大量蛋白尿型（MP）96例（23．9％）;高血压型（HT）36例（9．0％）;血管炎或新月体型（Cres）者31例（7．7％）。各类型的IgAN临床表现不同,表现为R-GH和Uab者,病理改变以系膜增殖为多见;MP者57％为系膜增殖,约26％为局灶节段硬化;HT型55％以上的患者为局灶节段硬化;膜增殖病变者主要表现为大量蛋白尿;轻微病变者多为孤立性肉眼血尿,也可见于无症状尿检异常和大量蛋白尿者。结论不同类型的IgAN在临床表现、病理等方面均有显著性差异,提示它在发病机制及治疗上应有所区别。     

Impact of interleukin-1 receptor antagonist and tumor necrosis factor-alpha gene polymorphism on IgA nephropathy

BACKGROUND: It is evident that cytokines play an important role in the pathogenesis as well as disease progression in IgA nephropathy (IgAN). The level of cytokine production is influenced by different genotypes that reflect gene polymorphism of the pertinent cytokine. Interleukin-1 receptor antagonist (IL-1ra) and tumor necrosis factor-alpha (TNF-alpha) gene polymorphism have been found to affect disease susceptibility and activity in several inflammatory diseases. However, the impact of these polymorphisms in IgAN patients has not previously been thoroughly studied. METHODS: We investigated 111 cases of biopsy-proven IgAN and 100 healthy, normal controls for their IL-1ra and TNF-alpha gene polymorphism. IL-1ra gene polymorphism was characterized as a variable number of tandem repeats of a 86 bp sequence within intron 2. Five alleles were identified and were designated as IL1RN*1, IL1RN*2, IL1RN*3, IL1RN*4, and IL1RN*5, corresponding to 4, 2, 5, 3, 6 repeats, respectively. A polymorphism in the promoter region of the TNF-alpha gene was also studied. This polymorphism involved a guanidine to adenosine transition at position -308 and was designated as TNF1 (-308G) and TNF2 (-308A). RESULTS: There were 54 male and 57 female patients with a mean age of 30.3 +/- 12.5 years and a disease duration of 66. 8 +/- 47.2 months. The mean duration of the follow-up period was 47. 3 +/- 32.6 months. In the patient group, the allele frequencies of IL1RN*1, IL1RN*2, IL1RN*3, IL1RN*4, and IL1RN*5 were 89.6%, 9.9%, 0%, 0.5%, and 0%, respectively, whereas the corresponding carriage rates were 100%, 19.8%, 0%, 0.9%, and 0%, respectively. An excessive carriage of IL2RN*2 was found in the patients when compared with normal controls (allele frequency, 9.9 vs. 2.5%, P < 0.0001). The allele frequencies of TNF1 and TNF2 were 94.1 and 5.9%, respectively, and the carriage rates were 99.1 and 10.8%, respectively, in the patients, which was not significantly different from those of normal controls. When the patients were stratified into mild and severe groups according to their initial presentation, none of the studied alleles correlated with the severity. However, patients with gross hematuria were associated with a higher carriage rate of TNF2 when compared with patients without gross hematuria (allele frequency, 15. 4 vs. 4.6%, P = 0.0552; carriage rate, 30.8% vs. 8.2%, P = 0.0272). Renal survival analysis revealed that the TNF2 carrier had a renal survival comparable with TNF2 (-) patients. However, the carriage of the IL1RN*2 allele was associated with a significantly poorer long-term outcome with a median survival time of 72 months, as compared with those without IL1RN*2 (134 months, P < 0.01). CONCLUSION: IL-1ra and TNF-alpha gene polymorphism may affect disease susceptibility as well as disease activity and long-term outcome in human IgAN. Treatment with an IL-1ra or IL-1 blocking agent may be relevant in those carrying the IL1RN*2 allele.     

Association of interleukin-1 receptor antagonist gene polymorphism with IgA nephropathy

It is evident that cytokines play an important role in the pathogenesis as well as disease progression of IgA nephropathy (IgAN). Several gene polymorphisms of the pertinent cytokines have an influence on the level of cytokine production. Interleukin-1 receptor antagonist (IL-1ra) gene polymorphism has been found to affect disease susceptibility and activity in several inflammatory diseases. In the present study, we analyzed polymorphism of the variable number tandem repeat (VNTR) of IL-1ra in patients diagnosed as having IgAN (n = 106) and normal controls (n = 74). The allele frequency of IL-1ra polymorphism in IgAN patients was not statistically different from that of the control group. There was no significant difference in the carriage rate of the two-repeat allele (IL1RN*2) between IgAN patients and the control group (8.5 vs. 6.8%). The carriage rate of IL1RN*2 was significantly higher in IgAN patients with severe proteinuria (>or=1.6 g/day) or increased serum creatinine level (>or=2.0 mg/dl; p < 0.05). Furthermore, the carriage rate of IL1RN*2 was significantly higher in patients with severe mesangial cell proliferation (p < 0.01). Our results suggest that IL-1ra polymorphisms are not associated with the development of IgAN in Japanese patients but the presence of IL1RN*2 may be associated with increased disease activity.     

Polymorphism in IgA nephropathy

Summary: IgA nephropathy (IgAN) is polyphormic in its clinical manifestation, course and prognosis. Patients with isolated IgA deposit in glomeruli tend to have a high incidence of macroscopic haematuria and carry a better prognosis. In contrast, patients with deposits of IgA and IgG and IgM have a higher incidence of nephrotic syndrome and hypertension. In parallel, patients with IgA and IgG and IgM tend to have more glomerulosclerosis and tubulointestitial lesions. Recently, the angiotensin converting enzyme (ACE) gene polymorphism and its association in disease risk provided interesting exploration leading us to speculate about a possible mechanism to explain the variation in the rate of progression of IgAN; although, the results are still controversial. The variability of plasma ACE concentration has been shown to be associated with an insertion/deletion polymorphism. The frequencies of ACE genotype in 177 Chinese patients with IgAN has been observed. We found that patients with IgAN showed a higher frequency of DD genotype than normal population. In contrast to the previous reports, we did not find any association between ACE genotype and the rate of progression of IgAN. As different genotypes of IL-1 receptor antagonist (IL-1 ra) are also responsible for the circulating levels of IL-1 ra, the polymorphism of IL-1 ra gene has been analyzed in 100 IgAN patients. There was no significant difference in the frequency of IL1RN*2 allele between normal subjects and IgAN. However, patients with recurrent macroscopic haematuria showed a higher carriage rate of IL1RN*2. Hereditable factors, in combination with a number of recognized environmental risk factors, are important determinants of the pathogenesis and natural history of IgAN. The notion that the gene polymorphism might be responsible for the clinical features and progression of IgAN is both intriguing and provocative. The lessons from previous multiple small size studies have produced conflicting results illustrating the need for observation of large numbers of cases in further studies to verify these observed associations.     

Interleukin 1 receptor antagonist and tumor necrosis factor-alpha gene polymorphism in patients with end-stage renal failure

End-stage-renal disease (ESRD) is a final result of various etiologies. Prognostic indicators leading to ESRD in chronic kidney diseases have been studied extensively, of which, genetic factors remain a subject of great concern. Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are potent proinflammatory cytokines that are involved in several chronic kidney diseases. Studies on cytokine gene polymorphism have revealed important information about the role of genetic factors in disease susceptibility and severity. Gene polymorphism of interleukin-1 receptor antagonist (IL-1ra) and TNF-alpha were determined in 297 ESRD patients and in 145 normal healthy controls. IL-1ra gene polymorphism was characterized as a variable number of tandem repeats of a 86 bp sequence within intron 2. Five alleles were identified and were designated as IL1RN*1, IL1RN*2, IL1RN*3, IL1RN*4, and IL1RN*5, corresponding to 4,2,5,3, and 6 repeats, respectively. A polymorphism in the promoter region of the TNF-alpha gene was also studied. This polymorphism involved a guanidine to adenosine transition at position -308 and was designated as TNF1 (- 308 G) and TNF2 (-308 A). The genotypes and allele frequencies were compared between patients and control group. The distributions of genotypes of IL-1ra and TNF-alpha did not differ significantly between ESRD patients and normal controls. Analysis of allele frequencies revealed a trend toward an increase in IL1RN*2 frequency (7.5% versus 3.8 %, p=0.064) and noncarriage of TNF2 in the patient group (7.2% versus 11.0%, p=0.076) when compared with the control group. When both alleles were considered together, the patient group had a significantly higher frequency of carriage of IL1RN*2 in combination with noncarriage of TNF2 (p=0.0468). We conclude that carriage of IL-1RN*2 and noncarriage of TNF2 allele appear to be poor prognostic factors in patients suffering from various chronic renal diseases that eventually enter end-stage renal failure.     

Polymorphism of the cytokine genes and IgA nephropathy

BACKGROUND: IgA nephropathy (IgAN) is a form of chronic glomerulonephritis of unknown etiology and pathogenesis. Cytokine gene polymorphisms regulate cytokine production and play a role in immune and inflammatory responses; these immunological responses thus are possibly involved in the etiology and pathogenesis of IgAN. METHODS: We studied by polymerase chain reaction (PCR) polymorphisms of important cytokine genes of inflammation interleukin-1 (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interleukin-1 receptor antagonist (IL-1Ra) in 167 patients with IgAN and 400 healthy blood donor controls. IgAN patients had been followed up for 6 to 17 (median 11) years from renal biopsy. RESULTS: Carriage of the IL-1beta allele 2 (IL1beta2) or IL-1Ra allele 2 (IL1RN*2) was associated with an increased risk of IgAN. These alleles were highly linked and the odds ratio (OR) of IgAN for carriage of both alleles was 1.8 (95% confidence interval 1.2 to 2.6; P = 0.002). Carriage of the TNF-alpha allele 2 (TNF2) was associated with a decreased risk of IgAN (OR 0.5, range 0.3 to 0.7; P = 0.001). The risk of IgAN was found to be highest in those carrying IL1beta2 and IL1RN*2 but not TNF2 as compared to those who did not carry both of these IL-1 cluster genes and were carriers of TNF2 (OR 5.0 (2.4-10.3); P < 0.001). None of the polymorphisms studied was associated with poor prognosis. CONCLUSION: Carriage of IL1beta2 and IL1RN*2 together with non-carriage of TNF2 is associated with increased susceptibility, but not with a prognosis of IgAN.     

Association of IL-1β, IL-1ra, and TNF-α gene polymorphisms in childhood nephrotic syndrome

We investigated the association between IL-1, IL-1ra, and TNF- gene polymorphisms and childhood nephrotic syndrome (NS). We analyzed the genetic polymorphism of IL-1, IL-1ra, and TNF- genes in 152 patients with childhood NS and 292 healthy adult controls. The C to T exchange at position –511 of IL-1 and the G to A at –308 of the TNF- gene were genotyped. Five alleles of the IL-1ra gene were identified and designated as IL1RN*1, IL1RN*2, IL1RN*3, IL1RN*4, and IL1RN*5, according to the variable number of tandem repeats in intron 2. The allele frequencies of IL-11 (-511C), IL-12 (-511T), TNF1 (-308G), and TNF2 (-308A) were 53.0, 47.0, 92.1, and 7.9%, respectively, in the childhood NS group. This was not significantly different from normal controls. In the childhood NS group, the allele frequencies of IL1RN*1, IL1RN*2, IL1RN*3, IL1RN*4, and IL1RN*5 were 90.8, 7.6, 1.6, 0, and 0% [IL1RN*1 odds ratio (OR)=0.296, P=0.0001, IL1RN*2 OR=3.902, P=0.0002]. A high allele frequency of IL1RN*2 and a lower allele frequency of IL1RN*1 were found in childhood NS, although there was no association with IL-1 and TNF-. A high allele frequency of the IL1RN*2 allele may affect disease susceptibility in childhood NS.     

IgA肾病和紫癜性肾炎患者白细胞介素-1受体拮抗剂基因多态性的功能研究

目的阐明白细胞介素１受体拮抗剂（ＩＬ１ｒａ）基因多态性对其功能的影响，论证ＩＬ１ｒａ基因型与ＩｇＡ肾病（ＩｇＡＮ）及紫癜性肾炎（ＨＳＰＮ）临床表型之间联系的机理。方法用ＰＣＲ方法对ＩｇＡＮ和ＨＳＰＮ患者ＩＬ１ｒａ基因型进行分析，从ＩＬ１ｒａ不同基因型患者获取外周血单核细胞，观察单核细胞经单核巨噬细胞集落刺激因子（ＧＭＣＳＦ）刺激后，ＩＬ１ｒａ、ＩＬ１α和ＩＬ１β的产生能力。结果无论是ＩｇＡＮ，还是ＨＳＰＮ患者，携带ＩＬ１ｒａ基因ＩＬ１ＲＮ＊２等位基因者其单核细胞ＩＬ１ｒａ的产生能力明显低于不携带该等位基因的个体，而ＩＬ１α和ＩＬ１β的产生能力与是否携带ＩＬ１ＲＮ＊２等位基因无关。结论ＩＬ１ｒａ基因多态性能对其功能产生影响。携带ＩＬ１ＲＮ＊２等位基因者其体内ＩＬ１ｒａ的产生能力存在缺陷。该结果为临床上根据ＩＬ１ｒａ基因型有针对地采取干预治疗奠定了基础。     

Polymorphisms in interleukin-1 beta and Interleukin-1 receptor antagonist genes are associated with kidney failure in Korean patients with type 2 diabetes mellitus

BACKGROUND/AIM: Cytokines play an important role in the pathogenesis of kidney diseases. The aim of the study was to investigate the impact of interleukin (IL)-1 cluster genes on diabetic nephropathy in Korean patients with type 2 diabetes mellitus (DM). METHODS: We investigated -511 C/T polymorphism of IL-1 beta and tandem repeat polymorphism in intron 2 of IL-1 receptor antagonist in type 2 DM patients with end-stage kidney failure as compared with patients without nephropathy. RESULTS: The IL1B2 allele was found more frequently in patients with kidney failure than in controls (57.4 vs. 46.1%, p < 0.05). An excessive homozygous carriage of IL1B2 was found in patients with kidney failure when compared with controls (30.5 vs. 18.3%, p < 0.05). The allelic frequency of IL1RN*2 was also higher in cases than in controls without nephropathy (8.4 vs. 2.8 %, p < 0.05). The carriage rate of IL1RN*2 was significantly associated with an increased risk of kidney failure (15.8 vs. 5.6%; OR 3.19, 95% CI 1.24-8.17). The risk of kidney failure was highest in those carrying both IL1RN*2 and IL1B2 (OR 3.90, 95% CI 1.34-11.40). CONCLUSION: IL1B2 and IL1RN*2 genotypes of the IL-1 cluster genes are associated with diabetic nephropathy in Korean patients with type 2 DM.     

Clinical features and natural history in adults with IgA nephropathy

Two different clinical syndromes might be observed at presentation in most patients with IgA nephropathy (IgAN): (1) an acute reversible episode of macroscopic hematuria or (2) asymptomatic urinary abnormalities. Patients in these groups differ by genetic markers, the severity of their histologic lesions, and the rate of progression to renal insufficiency. Macroscopic hematuria is more common in children, and its frequency decreases with increasing age. In our experience, most patients presenting in adulthood with macroscopic hematuria did not have proteinuria or microscopic hematuria prior to the episode of macroscopic hematuria, suggesting the onset of disease was indeed in adulthood. IgAN is not a benign disease. About 20% of patients reach end-stage renal failure after 20 years of clinical disease. Features generally associated with a poor prognosis include older age at onset, no history of recurrent macroscopic hematuria, hypertension, and consistent proteinuria. In some studies, men progressed more rapidly than women. Using the regression of Cox in the present study, the magnitude of proteinuria was the only clinical parameter that independently predicted progressive renal impairment.     

部分白细胞介素与IgA肾病易感性关联的Meta分析

目的本Meta分析旨在探讨白细胞介素（ILs）基因多态性与IgA肾病（IgA nephropathy,IgAN）发病风险的具体关联。方法检索范围从建库至2013年11月1日,计算机检索CISCOM、CINAHL、webofScience、Google学术、EBSCO、Cochrane Library、CBM和CNKI等中英文数据库,采用STATA 12．0软件进行Meta分析。结果本Meta分析最终纳入了7项病例对照研究,共包括1135例IgAN患者和1603例健康对照者。Meta分析结果表明,IL-1和IL-1RN基因多态性与IgAN风险的增加有关（IL-1：OR=1．33,950ACI=1．15～1．55,P〈0．001;IL-1RN：OR=1．32,95％CI=1．16～1．51,P〈0．001）。然而,在IL-6、IL-10和IL-22R基因多态性中并没有发现此关联性（均P〉0．05）。进一步根据种族不同进行亚组分析发现,无论是亚洲人群还是欧美人群,IL-1和IL-1RN基因多态性与IgAN风险的增加均存在明显相关性（亚洲人群：OR=1．58,95％CI=1．17～2．13,P=0．003;欧美人群：OR=1．53,95％CI=1．22～1．92,P＜0．001）。结论ILl和IL-1RN基因多态性可能与IgAN易感性增加有关,它可能是IgAN早期诊断和预后判定的重要分子标志物。